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Immunology > Beguiling Badass B Cells > Flashcards

Beguiling Badass B Cells Flashcards

1
Q

Rich Diversity of B cells stems from:

A

combinational diversity, junctional diversity, N & P nucleotides, somatic mutation

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2
Q

The Memory of B cells stems from:

A

somatic mutation and clonal selection of Fab, Ig heavy chain class switching of Fc, rapid response

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3
Q

CD79

A

(aka Igalphabeta), has ITAM, transmits signals from the BCR to the B-cell, is functional in the pre-B cell

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4
Q

3 molecules unique to the B cell

A

CD19, CD20, CD22

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5
Q

hematopoietic stem cells

A

B cell progenitor

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6
Q

first stage with specific B cell markers

A

Pro-B

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7
Q

first stage with a rearranged heavy chain

A

Pre-B

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8
Q

first stage with a functional BCR

A

immature B cell

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9
Q

where does final B cell maturation occur?

A

in the periphery

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10
Q

where does B cell development occur in the fetus

A

the fetal liver (pre-B cells appear at the end of the first trimester; by the second trimester, B cell differentiation occurs in the bone marrow, in the newborn >50% of B cells have CD5)

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11
Q

Characteristics of the stem cell B cell

A

no B cell specific markers, express CD34

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12
Q

characteristics of the Pro-B cell

A

B cell specific CD19, IL-7 dependent growth, heavy chain rearrangement

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13
Q

characteristics of the Pre-B cell

A

express pre-BCR, have rearranged heavy chain and surrogate light chain, signals via CD79, also has CD20 and IL-7R (still)

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14
Q

characteristics of the immature B cell

A

the first stage when the B cell can “sense” the antigenic milieu, B-cell tolerance occurs at this stage, expressed mIgM, CD19, CD20, Cd21, CD22, CD79

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15
Q

characteristics of the mature B cell

A

IgM and IgD, CD19, CD20, CD21, CD22, CD79

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16
Q

IL-7R

A

found only on the pro-B cell and the pre-B cell

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17
Q

IgD is found at what stage(s) of B cell development?

A

mature B cell

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18
Q

surrogate light chain

A

found on pre-B cells, is non-variant, is composed of VpreB and λ5

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19
Q

λ5

A

indicative of the pre-B cell

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20
Q

stage at which B cell tolerance occurs

A

immature B cell stage (must have fully formed BCR)

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21
Q

2 criteria the immature B cell is tested for

A
  1. productivity 2. self-reactivity
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22
Q

3 mechanisms of b cell tolerance (negative selection)

A
  1. B-cell receptor editing; 2. deletion; 3. anergy
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23
Q

BCR editing

A

occurs through the secondary VJ rearrangement at the Ig-light chain locus - accomplished via RAG enzymes (2-3 attempts)

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24
Q

deletion via apoptosis

A

death to B cells that are strongly reactive to self antigens of reactive to membrane bound antigens

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25
Q

anergy

A

is functional paralysis, occurs to B cells that are weakly reactive to self antigens or are reactive soluble antigens. Anergic B cells can exit to the periphery (but die quicker and respond poorly)

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26
Q

alternative B cell RNA splicing

A

allows co-expression of δ and μ heavy chains (μ is first on the RNA and δ is second)

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27
Q

products of peripheral B cell development

A

memory B-cells and plasma cells

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28
Q

total circuit time of B cells

A

12-24 hours

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29
Q

B cells that never meet their cognate antigen

A

usually die within B cell follicles

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30
Q

the spleen

A

monitors for blood borne pathogens

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31
Q

lymph nodes

A

monitor tissue-derived pathogens

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32
Q

MALT

A

monitors for pathogens entering via the mucosal portal

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33
Q

GALT

A

monitors for enteric pathogens (including Peyer’s patches)

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34
Q

WBC count

A

4,000-11,000 WBC/μl

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35
Q

lymphocyte count

A

1,000-4,000 lymphocytes/μl (15-40% of WBC)

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36
Q

secondary lymphoid organ T:B cell ratio

A

is generally 2:1 (T:B) – except the spleen that has more B cells than T cells

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37
Q

TDL

A

thoracic duct lymph - joins the blood before it recirculates to the heart; connects the lymphatic and blood circulations

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38
Q

L-selectin

A

CD62L only expressed by naive lymphocytes, interacts with GlyCAM1 (found on HEV); allows lymphocytes to enter lymph nodes form the blood, down regulated in activated effector lymphocytes

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39
Q

LFA1, VLA4, CD

A

bind to ICAM1, VCAM1, and LFA3 respectively; allow effector lymphocytes to enter inflamed tissues; VCAM is the most important for this extravasation process

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40
Q

difference between a primary and secondary follicle

A

a secondary follicle has a germinal center

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41
Q

Lymph Node vs. Spleen: T cell location

A

paracortex; PALS

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42
Q

Lymph Node vs. Spleen: naive B&T cell point of entry

A

HEV; central arteriole

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43
Q

white pulp

A

both B and T cell zones

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44
Q

Lymph Node vs. Spleen: macrophages and plasma cells

A

medullary cords; red pulp

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45
Q

Lymph Node vs. Spleen: marginal zone macrophages and marginal zone B-cells

A

sub-capsular sinus; marginal sinus – — important for T independent immune responses

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46
Q

sub-capsular/marginal sinus power

A

have B cells that an “sense” pathogens as they enter the spleen or lymph nodes

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47
Q

general lymphatic flow

A

afferent lymphatics –> sub-capsular sinus –> cortical sinus –> medullary cords –> efferent lymphatics

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48
Q

Activation of B cells requires how many triggers, and what are they

A

2 triggers: 1. antigen binding to the BCR; 2. helper T cells through CD40 (antigen specific, LINKED RECOGNITION) *a third cytokine based signal is helpful, but not necessary

49
Q

why is the necessary T/B cell interaction for B cell activation relevant?

A

it ensures that both B and T cells must be activated in order to create a response which decreases the likelihood of autoimmunity; “when self-tolerance is breached in both B and T cells”

50
Q

stopping of antigen specific lymphocytes occurs

A

in the T-cell zone

51
Q

linked recognition

A

does not require the T and B cell to bind to the same epitope on the antigen

52
Q

What happens after the B cell is activated by an antigen

A
  1. the B cell processes the antigen and presents it on an MHC Class II molecule; 2. the B cell up regulates CD40 and CD80/CD86; 3. the B cell presents this antigen to a T cell 4. the B cell CD80/CD86 (B7-1/B7-2) parley with CD28 (this causes CD40L to be up regulated on the T cell) 4. the B cell CD40 parleys with recently up regulated CD40L 5. ACTIVATION
53
Q

T cells in the T cell zone

A

are likely activated by antigens presented by dendritic cells, not B cells

54
Q

Fate of B cells activated in the T-cell zone

A
  1. form a primary focus, maturate into plasma cells, secrete antibodies; 2. travel to B-cell follicles, create a germinal center (guided by chemokines)
55
Q

somatic mutation

A

“random insertions of mutations in the hypervariable regions of the Ig”, occurs after antigen stimulation, key enzyme is AID

56
Q

germinal center, dark zone

A

where somatic mutation occurs –> creates a “panel of clonal offspring” with a “wide range of affinities for the antigen”

57
Q

affinity maturation

A

say yes to the antigen: B-cell style; occurs via somatic mutation and subsequent positive selection of b cell clones

58
Q

germinal center, light zone

A

contains follicular dendritic cells (DC with lots of antigen and immune complexes), where B-cell clone positive selection occurs

59
Q

what cells help B cells isotype switch from IgM

A

T follicular helper cells (mediated by AID, CD40L, and cytokines)

60
Q

AID

A

critical for B cell class switching and somatic mutation (same thing?? ask)

61
Q

plasma cell home, short term and long term

A

short: medullary cords and red pulp, long term: bone marrow (account for most of serum Ig

62
Q

memory B cells

A

class switched, lack IgD, higher affinity for antigens, lower threshold for activation, are in Go state, reside in the sub-capsular sinus and in the marginal sinus, can traffic to inflamed tissues, some are found in B-cell follicles

63
Q

IgD

A

not found on memory B cells

64
Q

the m in mIgM

A

“membrane”, as in membrane bound

65
Q

class switching is mediated by

A

the switch region at the 5’ end of each constant heavy chain gene (also is unique to heavy chains!)

66
Q

class switching occurs at what level and where

A

occurs at the DNA level and only one ONE chromosome (mediated by cytokines and AID)

67
Q

cytokines in class switching

A

determine which switch regions will rearrange - switching is irreversible, the VDJ region is upstream of the 2 switch regions and the intended constant heavy chain region

68
Q

IgA

A

T-reg, TGFβ; TH2, IL-5

69
Q

IgE

A

TH2, IL-4/IL-13

70
Q

IgG(1)

A

TH1, IFN-γ

71
Q

IL-6

A

drives plasma cells

72
Q

IL-2, IL-4

A

cytokines that act as the third “signal” for B cells

73
Q

primary immune response: IgM

A

peaks first, clinically indicates a recent infection (if high relative to IgG); increase in IgM occurs as a result of naive cell activation, IgM appears at 7 days, peaks at 10 days, and returns to baseline at 14 days

74
Q

primary immune response: IgG

A

peaks after IgM, is produced by a “minor subset of plasma cells” that switch from IgM secretion to IgG secretion

75
Q

secondary immune response: IgG

A

from the memory B-cells with high affinity IgG BCRs, IgG > IgM, immune response is quicker and stronger

76
Q

primary immune response

A

orchestrated in the T-cell zone

77
Q

three products of a successful secondary immune response

A
  1. effector T cells; 2. memory T/B cells 3. plasma cells and antibodies
78
Q

memory B-cells and germinal centers

A

some memory B-cells can generate new germinal centers (can produce further affinity maturation)

79
Q

the best antigens are in what form and why

A

those that are aggregated and/or presented in native (multivalent array) form; this is true because in order to activate a BCR, two or more IgM/D molecules must be “cross-linked to the antigen”

80
Q

CD73

A

is like CD3 on T cells; BCR activation (x-linking!) –> CD79 chain ITAMs (Ig-α, Ig-β) are phosphorylated –> recruit the tyrosine kinase ‘Syk’ –> causes phosphorylation of BTK –> activation of PLCγ2 –> DAG, IP3 –> NFAT, PKC, calcium, calcineurin, NFAT/PKC, NFκB/MAP kinase

81
Q

C3d

A

binds to CD21 (i.e. CR2) –> CD19 –> Fyn/Lyn;Vav/Pl-3K –> augmentation of B-cell signal 1

82
Q

antigen-antibody immune complex feedback

A

dampens B-cell signal via CD32 (FcRγIIb) –> phosphatase activation

83
Q

CD22

A

feedback pathway B-cell receptor: down regulates B-cell signaling

84
Q

CD32

A

FcRγIIb: low affinity Fc receptor

85
Q

CD81

A

something, something, amplification of BCR signal

86
Q

CD20

A

something, something, amplification of BCR signal

87
Q

CD40L is also known as

A

CD154 (this is a T-cell receptor)

88
Q

TI antigens

A

t-cell independent antigens

89
Q

T-cell dependent responses are characterized by what three things?

A
  1. class switching, 2. affinity maturation, 3. memory
90
Q

TI-1 ligands

A

act as a mitogen, trigger ALL B-cells polyclonally (ex - LPS); work via a toll like receptor, turn the B cell into a IgM warehouse

91
Q

TI-2 ligands

A

cross-link a large amount of BCRs, are polymeric antigens (ex. flagellin, Ficoll, dextran, bacterial polysaccharides); good at activating ‘primitive B cells’ (B-1 B cells – CD5) and marginal zone B cells

92
Q

mitogen

A

“a chemical substance that encourages a cell to commence cell division”, “Mitogenesis is the induction (triggering) of mitosis, typically via a mitogen”

93
Q

B-1 B cells

A

primitive B cells located in the peritoneal and pleural cavities, express the surface marker CD5

94
Q

TI antigens

A

do not create a response that has class switching, affinity maturation, or memory

95
Q

marginal zone B cells

A

are necessary to fight TI-2 antigens!

96
Q

allotypes

A

different members of a species will differ with one another with respect to which particular alleles of a given isotype they received from their parents

97
Q

T or F: different idiotypes can be detected in the sera

A

False - they have too low of a frequency (exceptions - patients with clonal expansion and mice with BCR transgenic B-cells

98
Q

antibody with the longest half life

A

IgG - 23 days

99
Q

antibody that can cross the placenta

A

IgG

100
Q

antibody that binds FcR

A

IgG (and IgA, weakly)

101
Q

antibody that can induce ADCC

A

IgG

102
Q

antibody that can neutralize toxin

A

IgG

103
Q

antibody found in milk

A

IgG, IgA

104
Q

antibody with anti-viral activity

A

IgG, IgA

105
Q

antibody with anti-bacterial properties

A

IgG, IgA (think lysosomes)

106
Q

antibodies that are agglutinators (best to worst)

A

IgM, IgA, IgG

107
Q

antibodies that fix complements

A

IgM and IgG (much less than IgM)

108
Q

antibodies with the highest and lowest molecular weights

A

IgM (900,000 Da), IgG (150,000 Da)

109
Q

antibodies with J and/or S chains

A

IgA (J and S), IgM (J)

110
Q

antibody found in secretions

A

IgA (also is intravascular)

111
Q

where is IgG found

A

intravascular and extravascular

112
Q

where is IgM found

A

mostly intravascularly

113
Q

IgG is good at

A

neutralizing toxins and viruses (blocking binding) and opsonization

114
Q

macrophages have receptors for

A

Fc (Fc receptor) and C3b (CR1)

115
Q

ADCC

A

via IgG binding to FcR on macrophages, basophils, NK cells, and eosinophils

116
Q

the first Ig a newborn makes

A

IgM (plateaus at 1-2 yrs.)

117
Q

IgA dimerization

A

increases its avidity –> powerful at neutralizing toxins (but doesn’t bind complement, does not do ADCC)

118
Q

know which cell produces Ig-h, Ig-κ, J-chain, and Poly-Ig receptor chains

A

huh, wtf? ask, poly Ig is from epithelial cells, j chain is from plasma cells, Ig-h & Ig-κ in plasma cell

Immunology (8 decks)

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